ArticleArthritis research & therapy2006
A cell-cycle independent role for p21 in regulating synovial fibroblast migration in rheumatoid arthritis.
Article in Arthritis research & therapy, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 26 citations in OpenAlex.
- Lactate programs CRIP1 protein lactylation to drive synovial proliferation in rheumatoid arthritis.JCI insight · 2026Article
- Cyclin-dependent kinase inhibitor-1 deficiency enhances bone destruction in a mouse model of arthritis.Bone reports · 2025Article
- MyD88 dimerization inhibitor ST2825 targets the aggressiveness of synovial fibroblasts in rheumatoid arthritis patients.Arthritis research & therapy · 2023Article
- Liquid biopsies to guide therapeutic decisions in rheumatoid arthritis.Translational research : the journal of laboratory and clinical medicine · 2018Review
- SIRT1 promotes tumor-like invasion of fibroblast-like synoviocytes in rheumatoid arthritis via targeting TIMP1.Oncotarget · 2017Article
- Orphan nuclear receptor NR4A2 induces transcription of the immunomodulatory peptide hormone prolactin.Journal of inflammation (London, England) · 2015Article
- Activated protein C inhibits proliferation and tumor necrosis factor α-stimulated activation of p38, c-Jun NH2-terminal kinase (JNK) and Akt in rheumatoid synovial fibroblasts.Molecular medicine (Cambridge, Mass.) · 2013Article
- A pathway analysis applied to Genetic Analysis Workshop 16 genome-wide rheumatoid arthritis data.BMC proceedings · 2009Article
- Synovial fibroblasts spread rheumatoid arthritis to unaffected joints.Nature medicine · 2009Article
- Enhanced susceptibility of cyclin kinase inhibitor p21 knockout mice to high fat diet induced atherosclerosis.Journal of biomedical science · 2009Article
- Developments in the synovial biology field 2006.Arthritis research & therapy · 2007Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Rheumatoid arthritis (RA) is characterized by synovial hyperplasia and destruction of cartilage and bone. The fibroblast-like synoviocyte (FLS) population is central to the development of pannus by migrating into cartilage and bone. We demonstrated previously that expression of the cell cycle inhibitor p21 is significantly reduced in RA synovial lining, particularly in the FLS. The aim of this study was to determine whether reduced expression of p21 in FLS could alter the migratory behavior of these cells. FLS were isolated from mice deficient in p21 (p21(-/-)) and were examined with respect to growth and migration. p21(-/-) and wild-type (WT) FLS were compared with respect to migration towards chemoattractants found in RA synovial fluid in the presence and absence of cell cycle inhibitors. Restoration of p21 expression was accomplished using adenoviral infection. As anticipated from the loss of a cell cycle inhibitor, p21(-/-) FLS grow more rapidly than WT FLS. In examining migration towards biologically relevant RA synovial fluid, p21(-/-) FLS display a marked increase (3.1-fold; p < 0.05) in migration compared to WT cells. Moreover, this effect is independent of the cell cycle since chemical inhibitors that block the cell cycle have no effect on migration. In contrast, p21 is required to repress migration as restoration of p21 expression in p21(-/-) FLS reverses this effect. Taken together, these data suggest that p21 plays a novel role in normal FLS, namely to repress migration. Loss of p21 expression that occurs in RA FLS may contribute to excessive invasion and subsequent joint destruction.
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